Case History

Cardiology, coagulation

Patient with acute myocardial infarction with STEMI

On October 15, 2005, at 2:00 a.m., a 61-year-old man was admitted to our emergency ward. He reported severe left thoracic chest pain at rest with radiation tothe neck and left arm that began the day before at 10:30 p.m., i.e., 3 1/2 hoursbefore admission and lasted for 2 hours.

In the past weeks he experienced similar episodes of milder intensity during exertion. There were no concomitant vegetative symptoms or dyspnea. He had never suffered from palpitations, dizziness, or syncope.

Cardiovascular risk factors were arterial hypertension, hypercholesterinemia, and insulin-dependent diabetes mellitus since 1984. The patient had quit smoking 2 years ago (20 packyears).

Medications on admission were nifedipine 20-mg tablet and simvastatin 20-mg tablet once daily and metformin 850-mg tablet twice daily.

The precordial leads showed monophasic ST-segment elevations in V1–V3. Besides, there were ST-segment elevations up to 0.1 mV in lead aVL. These ST-segment elevations were superimposed on an RBBB. In addition, there were ST-segment depressions in leads II, III, and avF and in the precordial leads V5 and V6. Besides, there wasa first-degree atrioventricular block.

Cardiopulmonary examinationThere were no findings of congestive heart failure, no third or fourth heartsound, no cardiac murmurs, and pulse rate 80 bpm—normal pulmonary findings.

Sodium 139 (135–145 mmol/L)Potassium 5.65 (3.5–4.8 mmol/L)Creatinine 0.99 (<1.3 mg/dL)Urea 85 (<45 mg/dL)Creatine kinase 375 (<174 U/L)cTnT 0.26 (<0.03 μg/L)C-reactive protein 3.0 (<5 mg/L)WBC 18.52 (4.0–10.0 cells/nL)Hemoglobin 14.1 (13–17 g/dL)Platelets 303 (150–440 cells/nL)

Biochemistry

• Medical treatment

• Immediately after diagnosis of STEMI, the patient received 600 mg clopidogrel

• and 500 mg aspirin orally as well as 5000 units unfractionated heparin intravenously.

• In addition, the glycoprotein (GP) IIb/IIIa inhibitor tirofiban was administered in the emergency room before coronary angiography.

• After percutaneous coronary intervention (PCI), tirofiban was continued for 48 hours.

• Coronary angiography

• Coronary angiography was performed immediately, revealing a severe coronary three-vessel disease with a total occlusion of the proximal left anterior descending artery (LAD). The LAD could be successfully recanalized.

• On left ventricular angiography the left ventricular function was severely impaired.

• PCI resulted in an incomplete reperfusion of the infarct-related artery (thrombolysis in myocardial infarction (TIMI) flow grade 2).

Inhospital course

During coronary angiography, the patient developed cardiogenic shock.

After implantation of an intraaortal balloon pump he was monitored and had an uneventful stay on our intensive care unit.

Troponin T values were determinedimmediately after PCI and every day until discharge.

On admission, cTnT level was 0.26 μg/L, which was nine times above the reference limit.

Following coronary angiography,cTnT levels increased to 2073 times upper limit of normal and then declined rapidly.

This release kinetic is typical for an early successful reperfusion of an occluded coronary artery.

On Day 4, a gadolinium-enhanced magnetic resonance imaging (MRI) was done in order to assess left ventricular function and to estimate the infarct size.

The infarct size was measured by addition of the volumes of late enhancement in contiguous short-axis slices of known thickness. Absolute infarct mass and relative infarct size was calculated.

The infarcted area was quantified to more than 140 g

cTn and infarct size

Follow-up

• The patient was discharged from our hospital after 10 days on October 25.

• On follow-up, he reported limited physical exercise capacity and shortness of breath at exercise classified as functionalNYHA(New York Heart Association) class III.

• There was no evidence for recurrent myocardial ischemia or clinical restenosis.

• Transthoracic two-dimensional echocardiography demonstrated an ejection fraction of only 20%. Hence, he received a dual-chamber implantable cardioverter defibrillator for primary prophylaxis of sudden death according to the MADIT-II-trial criteria.

How many troponin measurements do we need in patients with

STEMI?

• Only in patients with onset of symptoms 4–6 hours before admission and in whom admission troponin is still negative, another blood sample should be obtained 6–9 hours later.

• In patients receiving thrombolytic therapy an additional troponin measurement 60–90 minutes after start of treatment may complement other noninvasive

• tools for noninvasive estimation of reperfusion success.• Finally, the last measurement between 72 and 96 hours after

the index event allows estimation of infarct size.

Cases from clinical praxisCases from clinical praxis• 65year old man, AP, 30 minutes pain in

chest,

• i.v. aplication of nitrates – pain is lost

• cTn normal values

• ECG tachycardia without ST segment elevation or depresion

• What can we do? Hospitalize or not?

Patient with acute myocardial infarction with non STEMI

•A 65-year-old,male, retired engineer with a history of hypertension and ongoing tobacco use presented to the emergency room with chest pain.

•He woke that morning with a pressure sensation in his mid-chest associated with diaphoresis and nausea. He got out of bed, but pain worsened with exertion, and was then associated with lightheadedness. An ambulance was called.

•After receiving an aspirin and two sublingual nitroglycerins, he became pain-free. He was transported to the local hospital for further evaluation.

Investigation inED

•Heart rate was 90 and regular, blood pressure 162/88, and oxygen saturation 98% Estimated jugular venous pressure was 7 cm and no thyromegaly was noted. Lungs were clear to auscultation bilaterally.

•Cardiac examination was notable for normal S1, physiologically split S2, and presence of an S4. No murmurs were heard.

•A 12-lead electrocardiogram (ECG) showed normal sinus rhythm with left ventricular hypertrophy and 1-mm ST-segment depression in leads V2–V4.

•Chest X-ray showed no cardiopulmonary abnormalities.

Patient with acute myocardial infarction with non STEMI

• Laboratory investigation 4 hrs after symptoma onset normal blood counts and

chemistries except of:

cTnT = 0.16 ng/ml (URL = 0.1 ng/ml)CK-MB = 14 ng/ml (URL = 9 ng/ml)

12 hours after symptoma onset (peak)

cTnT = 0.22 ng/ml, CK-MB = 20 ng/mlcTnT = 0.22 ng/ml, CK-MB = 20 ng/ml

Then concentrations slightly fall

• The patient remained pain-free and was admitted to the cardiac intensive care unit for further management. In the intensive care unit, the patient was treated with enoxaparin and eptifibatide

• in addition to aspirin, β-blocker, statin and angiotensin-converting enzyme (ACE) inhibitor.

• The patient underwent cardiac catheterization on hospital day 2, which revealed a 95% hazy obstruction of the mid left anterior descending (LAD) artery, suggestive of fresh thrombus.

• He was given clopidogrel 600 mg and then underwent percutaneous implantation of a drug-eluting stent to the LAD lesion with a final result of <25% luminal obstruction.

• He remained on an eptifibatide infusion for 18 hours postprocedure.

• The remainder of his hospitalization was unremarkable andthe patient was discharged on hospital day 4 to cardiac rehabilitation.

Follow up

Summary of the case

• Elevated troponin levels identify patients with ACS who are at higher risk and who derive particular benefit from aggressive therapies such as use of low molecular weight heparin, glycoprotein IIb/IIIa inhibitors,and early invasive strategies.

Man 49 r., suspect AIM. EKG normal S-CK S-AST (kat/l)3 hod 21,5 1,524 hod 9,6 0,6548 hod 3,2 0,4

Can ve confirm diagnosis of AIM ? Which other markers we can invesdtigate to support the diagnosis ?What is the cause of elevation of enzymes ?

↑↑CK (in admission). TnI a CKMB – No AIM

Intramuscular aplication of analgetics (rhabdomyolysis elevated CK

Case II

Case III• Woman 51 let – mild hypertension, 2 hours before visit ED –chest pressure,

statin therapy, refused therapy for hypertension, avid runner, previously without such difficulties, difficulties at rest and released in pain and neck

• ECG – small ST segment a change of T-wave – mild ischemia

• CTnT = 0,04 μg/l (cut off 0,01 μg/l), next analysis -

0,32 μg/l a 0,76 μg/l , then decreasing into the normal values

• MRI – 3 % LK – subendocardial inner wall –“microinfarct“

Dg. AIM 2

Treatment Non-STEMI – statins, ACE inhibitors, β – blockers

Patient with CAD and renal insuficiency

• A 75-year-old man with chronic kidney disease on hemodialysis for the past 6 months and a history of hyperlipidemia, hypertension, and adult-onset diabetes mellitus presents to the emergency department with a chief complaint of increasing dyspnea in the last 24 hours.

• He appears pale and diaphoretic. His heart rate is 101, blood pressure 90/55, respirations 21, and his oxygen saturation is 90%

Cardiological examination

- regular rhythm with an S4. His lungs are clear to auscultation bilaterally.

- A 12-lead ECG shows normal sinus rhythm with Q waves in leads II, II, and aVF consistent with an old inferior infarction. No acute ST-segment or T-wave abnormalities were noted.

Other examination and follow up• CTn = 0.23 ng/mL (URL = 0.10 ng/mL) and CK-MB of 4 ng/l (URL = 9 ng/ml)Investigation of noncardiac etiologies, including chest X-ray, basic chemistries,and a ventilation–perfusion scan, was negative.

• The patient was given aspirin,lopressor, and intravenous UFH, and was admitted for further evaluation.

• On hospital day 2, an echocardiogram revealed an ejection fraction of 40% with inferior hypokinesis.

• His troponin peaked at 0.42 ng/mL 12 hours after admission, and then trended down.

• On hospital day 3, cardiac catheterization revealed a 75% distal right coronary artery lesion that was treated with a drug-eluting stent with good results.

• The patient was started on a statin, oral β-blocker, and clopidogrel. An ACE inhibitor was started as well but had to be discontinued due to hyperkalemia of 6.1 ng/mL two days after initiation.

• Patient was discharged on hospital day 5 without events.

Discussion of case

• The prevalence of CAD in patients with renal insufficiency is high and is a major cause of morbidity and mortality.

• In patients on dialysis, the prevalence of CAD is estimated at 40% and cardiovascular disease accounts for almost 50% of deaths in patients with chronic renal insufficiency

cTn and renal failure• Cardiac troponins are very specific markers of myocardial necrosis.

• 50% of asymptomatic patients with renal failure, whether acute, chronic, or end stage, have elevated troponin levels.

• Troponin I is elevated in 7% of patients with advanced renal failure whereas• troponin T is elevated between 17 and 53% of patients with renal failure

• A higher proportion of troponin T (7% versus 3.5% troponin I) exists freely in the myocyte cytoplasm while the rest is bound within the sarcomere and therefore greater release of the unbound cytosolic troponin T may account for the higher specificity of troponin I in patients with renal failure.

Troponin elevations in ESRD

• Uremia-induced skeletal muscle reexpression of cardiac troponin T, clinically silent micro-infarctions, left ventricular hypertrophy, and subclinical volume overload and heart failure

cTn and renal failure

• In asymptomatic patients with renal dysfunction, troponin elevation has been shown to predict a two- to fivefold increase in all-cause mortality

• suggesting a role for troponin in the clinical risk assessment of patients with renal disease.

Patient with CAD and diabetes

• A 54-year-old diabetic man noted vague epigastric discomfort and nausea after lunch.

• Four hours later, having no symptom relief from

over-the-counter antacids, he drove himself to the local emergency department for furtherevaluation.

• On arrival in triage, he was noted to be pale and diaphoretic.

Other examinations and follow up•Heart rate was 106 and blood pressure 92/50.

• He was given an aspirin and three sublingual nitroglycerins without substantial relief of his discomfort.

• A 12-lead ECG showed 3-mm ST-segment elevation in V2–V5. Urgent cardiology consultation was obtained and the patient was transferred to a local tertiary facility for cardiac catheterization.

• Coronary angiography revealed a total occlusion of a large left anterior descending artery, which was treatedwith a drug-eluting stent with resolution of symptoms and ST-segment elevations.

•He received a clopidogrel load of 600mg and remained on abciximab for another 12 hours post-procedure.

•En route, blood samples were drawn and patient was initiated on intravenous UFH and abciximab infusions.

•Testing of his pre-catheterization blood samples revealed a troponin T of 2.3 ng/mL (URL = 0.10 ng/mL) and a CK-MB of 24 ng/mL (URL = 9 ng/mL).

Cardiac enzymes peaked at 6 hours post-revascularization and then trended down. The patient had no recurrent symptoms.

• An echocardiogram showed moderate anteroapical hypokinesis with an estimated ejection fraction of 40%. The patient was started on daily aspirin, statin, β-blocker, and ACE inhibitor.

•He was discharged a few days later to cardiac rehabilitation.

A 48-Year-Old Cocaine Userwith Chest Pain

• A 48-year-old male presented to the emergency department with constant, “squeezing,” left sided and substernal chest pain following a night of partying with friends that included ingestion of alcohol and crack cocaine.

• He stated that the pain started acutely around 2:30 am while he was sleeping and was temporarily relieved following the ingestion of two nitroglycerin tablets at home.

• He was not short of breath or diaphoretic. The pain did not radiate, was nonpleuritic, and was not associated with exertion but was similar in character to the chest pain he experienced when admitted last month for a myocardial infarction.

• Improvement, but not resolution, of the pain was noted by the patient following administration of an aspirin, nitroglycerin, and metoprolol.

A 48-Year-Old Cocaine Userwith Chest Pain

• His past medical history is significant for a non-ST-segment elevation myocardial infarction suffered last month following the ingestion of crack cocaine. Cardiac catheterization at that time revealed essentially normal coronary arteries that required no intervention.

• An echocardiogram completed 2 months prior to this presentation revealed a normal ejection fraction, mild left ventricular hypertrophy, and no wall motion abnormalities.

• His medical history is also noteworthy for a diagnosis of small cell lung carcinoma that was treated with radiation and chemotherapy 7 years ago. He had metastasis involving his brain with multiple strokes and transient ischemic attacks secondary to whole-brain radiation in 1998. He has only mild residual deficits secondary to these multiple strokes. Additionally, he has hypertension and a history of substance abuse.

• His current medications include lisinopril, metoprolol, and atorvastatin.

Other examinations and follow up• blood pressure was 170–200 systolic and 90–104 diastolic with a heart

rate in the 60s and a respiration rate 20.

• oxygen saturation was 98%; temperature, 97.38F; and he appeared to be in mild distress.

• Diminished breath sounds were found on auscultation of the bilateral

upper lobes of his lungs, while the remainder of his lung and cardiovascular examination was unremarkable.

• No neck vein distention or lower extremity edema was seen and his abdomen was benign.

• Neurologic examination was normal.

• An EKG demonstrated a normal sinus rhythm.

• An echocardiogram completed the following morning demonstrated a normal left ventricular ejection fraction, no wall motion abnormalities, mild left ventricular hypertrophy, left atrial enlargement, a small pericardial effusion, and insufficiency of the aortic, mitral, and tricuspid valves.

Laboratory investigation

Discussion • The most important diagnostic decision to make in the setting of

chest pain following cocaine use is to determine whether the patient has actually sustained acute myocardial damage that requires prompt medical and surgical management.

• It is estimated that only 6% of persons who present to the emergency department with chest pain after the ingestion of cocaine will actually have an acute myocardial infarction.

• This small percentage of persons likely to have myocardial ischemia together with the fact that distinguishing chest wall and skeletal pain from acute myocardial ischemia is challenging because three of the main criteria for a diagnosis of AMI are similar in both settings.

Discussion

• The etiology of acute myocardial infarction secondary to cocaine use is thought to be caused by an imbalance of the increased demand placed on the cardiovascular system by an elevation in heart rate and blood pressure versus the decreased delivery of oxygen secondary to coronary artery spasm.

• The decreased oxygen delivery via the coronary arteries has also been theorized by some to be

exacerbated by enhanced atherosclerosis, increased platelet aggregation, and thrombus formation within the coronary arteries after cocaine ingestion

Coagulopathies

Treatment of thrombosisTreatment of thrombosis

Coumarins (Vit K antagonists)

-Oral anticoagulnts, treatment of AMI, thrombosis.

- interindividual variability.

- Incorrect dosing – life threatening complications (overdose – bleeding, incomplete prophylaxis – lower dose)

Blood coagulation investigation – INR values

VKORC1 polymorphism – coumarin sensitivity

Variability of CYP2C9 - different rate of coumarine elimination.

LOWMEDIUMHIGH

HIGHMEDIUMLOW

HIGHMEDIUMLOW

Coumarin sensitivity

Metabolic state

Coagulopathies

Antivenom 12 hours after ED visit

Coagulopathies